Stimulation and inhibition of PGI2 synthetase activity by phospholipids (PL), cholesterol esters (CE), unesterified fatty acids (UFA) and lipoproteins (LDL and HDL).
We investigated the influence of different lipids on the transformation of PGH2 to PGI2 by the microsomal fraction of pig aorta. Phospholipids and cholesterol esters obtained from animals fed prenatally a linoleic acid rich diet stimulated the PGI2 formation. However, when obtained from animals fed prenatally a linoleic acid deficient diet, phospholipids and cholesterol esters inhibited PGI2 production. Unesterified fatty acids are potent inhibitors at 1 mM. The degree of inhibition was dependent on the length of the carbon chain and the number of double bonds in the UFA molecule. We found further that lipoproteins modified the PGI2 formation at physiological concentrations. The amount of hig density lipoprotein cholesterol had a positive correlation with the activity of PGI2 synthetase, whereas the amount of low density lipoproteins cholesterol had a negative one.
D000818:Animals; D002788:Cholesterol Esters / Q000494:pharmacology*; D016861:Cyclooxygenase Inhibitors; D004032:Diet; D011464:Epoprostenol / Q000096:biosynthesis; D005230:Fatty Acids, Nonesterified / Q000494:pharmacology*; D006801:Humans; D008041:Linoleic Acids / Q000008:administration & dosage / Q000172:deficiency; D008075:Lipoproteins, HDL / Q000494:pharmacology; D008077:Lipoproteins, LDL / Q000494:pharmacology; D010743:Phospholipids / Q000494:pharmacology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D051381:Rats; D013552:Swine
D002788:Cholesterol Esters; D016861:Cyclooxygenase Inhibitors; D005230:Fatty Acids, Nonesterified; D008041:Linoleic Acids; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D010743:Phospholipids; D011464:Epoprostenol; D011451:Prostaglandin-Endoperoxide Synthases